Sinus Tachycardia

It’s one of the first arrhythmias we all learn and it seems so simple. Sinus tachycardia is a regular rhythm faster than 100 bpm with a sinus P-wave before each QRS, right?

Well, let’s examine some of its finer points.

Figure 1. This is not sinus tachycardia.

I’m going to tell you that the ECG above does not show sinus tachycardia.

It’s from an 85 year old female who presented with shortness of breath and a cough for three weeks. She was initially diagnosed with pneumonia but did not improve on antibiotics so she presented to the ED. She appeared very healthy for her age and while her BP was 115/55 mmHg, her respiratory rate at rest was 32 /min (yet surprisingly unlabored) and SpO2 93% on 2 Lpm (no pulmonary Hx). Her temperature was 36.9 C (98.4 F).

Unsurprisingly, CT angiography show a large PE in her right main pulmonary artery.

So why doesn’t her ECG show sinus tachycardia? Let’s start by talking about her heart rate.

The upper rate

You may think I’m trying to trick you because her heart rate is above 150 bpm. Nope. There is a misguided notion that a narrow-complex tachycardia in an adult > 150 bpm constitutes “SVT,” implying a re-entrant mechanism involving the AV-node that can be remedied with adenosine. As we have debunked many times before, sinus tachycardia does not have a clear upper boundary for its rate. Below are some examples of true sinus tachycardia in adults.

Figure 2. If a heart rate of 150 bpm defines SVT, this 21yo M who presented after smoking an unknown substance is only 1 bpm away from receiving adenosine. That line of thinking demonstrates a deep misunderstanding of the physiology of re-entrant tachycardias and the mechanism of adenosine.

Figure 3. Oh good, a heart rate over 150 bpm; clearly the problem is cardiac [Sarcasm]. The patient was septic and febrile.

Figure 4. Sinus tachycardia, this time decidedly over 150 bpm. Again, this was from a patient who was febrile with sepsis.

Figure 5. Sinus tachycardia in a 59yo M with respiratory distress due to a COPD exacerbation.

Figure 6. Sinus tachycardia at 172 bpm in a 79yo F experiencing an anaphylactic reaction. According to the old 220-age rule her maximum heart rate should have been around 140 bpm, but this is confirmed sinus tachycardia with several tracings showing a gradual resolution of her rate as her symptoms diminished.

Alright, we get the point, the sinus node can discharge as fast as it needs to depending on the patient’s condition. Sure, the maximum heart rate an individual can maintain is limited by their age and health, but it does not conform to strict rules like “>150 bpm = SVT” or “maximum HR = 220 – age.” This is all stuff we have talked about before [1][2][3][4].

With that resolved, there is something else I want to discuss regarding the rate of sinus tachycardia, and it’s a topic most people assume is set in stone: the lower limit.

The lower rate

Of course there’s a reason we do that. When we’re first learning arrhythmias (or dysrhythmias, I don’t care what you call them) we’re completely overwhelmed by all the complicated AV-blocks, fibs, flutters, and whatnot. We need simple rules, so 100 bpm is chosen as the lower limit of sinus tachycardia because it’s a round number and easy to remember and in all the books we read and all the protocols and guidelines we follow and everyone knows it. It’s also easy to measure on the ECG because it corresponds to an RR-interval of 600 ms (exactly 3 big boxes).

Figure 7. Sinus tachycardia at just over 100 bpm.

But once we’ve learned the “rules” and are competent at basic rhythm diagnosis, few people look back at this simplest of rhythms and ask if that number actually makes sense.

The problem with trying to define a “normal” resting heart rate is that it varies from person to person. The discharge rate of the sinus node is the result of a complex interplay between the sympathetic and parasympathetic nervous systems, and anything from your age to the time of day to how recently you’ve eaten to what medications you’re on can affect that value.

So, for whom is a resting heart rate of 99 bpm normal? How about 95 bpm? 92 bpm?

I’d argue: not many healthy people, most of the time.

As a result, I’d also argue that we need to change our definition of “sinus tachycardia.” It turns out I’m not the only one who thinks so. Dr. Palatini’s reasons are a bit different from mine, however. He is looking at this from a epidemiological perspective as it would apply to the outpatient setting. There are studies showing that higher resting heart rates correlate with increased morbidity and mortality, so folks who subscribe to Dr. Palatini’s line of thinking are looking to identify patients at higher risk of bad outcomes on a timescale of years. Working in prehospital and emergency medicine, I’m worried about the next few hours and days.

Fortunately, despite our different priorities, I think we like roughly the same numbers.

I’ve personally chosen my cutoff as 90 bpm in adults. While there is some science behind that value (see the references in the above link), most of the studies of resting heart rate that I’ve seen are done outside of the acute care setting for obvious reasons. I’ve mostly chosen 90 bpm as my cutoff because it feels right based on my experience. That doesn’t mean I consider 89 bpm “normal” and 90 bpm “abnormal”â€”88bpm is way too fast for an elderly man on metorpolol and cardizem, for instanceâ€”but when forced to choose an arbitrary cutoff to define sinus tachycardia in adults, I like that number a heck of a lot better than 100 bpm. Maybe it should be 85 bpm in men and 88 bpm in women, or 87 in men and 89 in women, but I’ve decided to pick one and for now it’s 90 bpm.

I like using a lower value because it greatly enhances my sensitivity for picking up issues causing the elevated heart rate without a detrimental increase in false positives. Sure, there are certainly more people who meet the criteria for sinus tachycardia when I lower the bar, but that doesn’t bother me.

If an adult is sitting in front of me with a heart rate over 90 bpm, I want to know the reason why. The differential for sinus tachycardia is long, but it’s usually easy to cross off the major players. Often their heart rate is mildly elevated because they have a fever. Or it’s because they’re anxious. Or they just stood up. Or that woman with shoulder pain experienced a spontaneous rupture of an undetected enlarged spleen and that’s why her heart rate is 96 bpm.

However serious or benign the cause ends up being, however, if someone has a heart rate over 90 bpm, I go searching for a cause. It doesn’t have to be exhaustive, and I’m certainly not advocating excessive testing and workup of patients with mildly elevated heart rates, but when I see someone who is resting in bed with minor complaints and their heart rate is clicking along at 94 bpm for no apparent reasons, I broaden my history and exam just a little to try and find the culprit.

Since we work in a field where uncommon but serious diagnoses are both expected and our reason for existing, I think it’s worth the effort.

Figure 9. Mild sinus tachycardia in a 25yo F with a low-grade fever. Typically unimportant, the “abnormal” heart rate was key in this case because the patient was immunocompromised and oral temperature readings did not register a fever. Her persistent elevated HR in the 90’s prompted a rectal temperature, which registered at 38.2 C (100.8 F).

Back to our case

Let’s get back to that first ECG in Fig. 1. How do I know that it isn’t sinus tachycardia? From looking at the ECG in isolation, I don’t. It meets all the morphological criteria and the patient’s presentation certainly fits; though 158 bpm seems a bit too fast for an elderly patient who appears wellâ€”even if she does have a large PE. So here’s what happened.

I looked at her chart and it turned out she had an ECG performed on arrival to the ED one hour prior:

Figure 10. In hindsight this ECG shows true sinus tachycardia with a single obvious PAC.

Perplexed by the drastic change in rate over the past hour I went to the patient’s room and essentially asked, “What’s your deal, lady?”

She denied any change in symptoms while in the ED and I noted her heart rate was in the low 100’s.

We chatted for a few minutes then suddenly the alarm beeped (not the super bad Crisis alarm, just the standard Warning), and I looked up to see her heart rate was back into the 150’s. She still denied any symptoms.

Figure 11. This strip shows a narrow-complex tachycardia with a sinus-appearing P-wave before each QRS, but the tachycardia is abrupt in onset and initiated by a PAC.

The above strip in Fig. 11 is proof that the tachycardia on her first ECG is not sinus in origin… at least not in the conventional sense.

Note that there is an abrupt change in rate from approximately 105 bpm to about 160 bpm. While there is still a P-wave in front of every QRS and the P-wave is nearly identical to the sinus P-waves at the start of the strip, sinus tachycardia does not start (or end) abruptly. Additionally, the tachycardia is initiated by a PAC, further confirming it is not typical sinus tach.

Looking back at Fig. 10, you’ll see there is not only one apparent PAC preceding QRS #11 (with an inverted morphology in lead II),Â but the P-waves before QRS complexes #4, 8, and 16 are also prematureâ€”though of seemingly normal shape.

Our patient continued to have dozens of paroxysm of this sudden tachycardia before it was brought under control with administration of a beta blocker. Here are some more initiations of the tachycardia; sorry I didn’t grab any terminations for some reason. If anyone out there is a rhythm expert feel free to dissect them and let me know what you see.

Figure 12.

Figure 13.

Figure 14

Figure 15. Note the short run of aberrancy at the start of the tachycardia.

What we have is an abrupt-onset, narrow-complex tachycardia that is initiated by a PAC. There is a long RP-interval (time from the R-wave to the next P-wave) with an upright P-wave very much resemblingâ€”though admittedly slightly different fromâ€”the true sinus P-waves.

Our patient is possibly experiencing paroxysms of something called sino-atrial nodal re-entrant tachycardia (SANRT). It is also called sino-atrial nodal re-entry tachycardia, sinus node re-entry tachycardia, SA re-entrant tachycardia, or any combination of similar terms. The nomenclature of this arrhythmia is a real mess.

What’s key is that SANRT is a re-entrant tachycardia (like AVNRT), but instead of circling around the AV-node, the electrical circuit rings the area surrounding the sinus node. I say that the patient is possibly experiencing SANRT because she could also be experiencing another form of re-entrant atrial tachycardia arising from near the sinus node but not actually circling it, but that distinction can only be made in the EP lab and does not matter to us.

The important point is that not everything that looks like sinus tachycardia is sinus tachycardia. Even the most seemingly clear-cut of cases can have a surprising twist, so don’t underestimate our old friend sinus tach. What are the hallmarks of sinus tachycardia?

Heart rate > 90 bpm (or 100 if you’re a conformist)

Upright P-waves in I, II, and aVF; often III and/or aVL as well; inverted in aVR

PR-interval of 120 (give or take a little bit) or greater; usually less than 300 ms

Gradual changes in rate, especially in response to activity, rest, or treatment

I’m going to leave you with one final ECG that does not show sinus tachycardia. If you can figure out the diagnosis you’ll also know the next topic we’re going to cover in this series.

Figure 16. This also does not show sinus tachycardia.

Further Reading

I’ve got another case of even more classic-appearing SANRT somewhere in a pile on my desk from a patient experiencing spells of palpitations that multiple physicians told her were just “anxiety,” but I can’t find it at the moment. I’ll update this page when I do.

Ken Grauer58 Year Old Male, Workout Worry@ Eli — I don’t see AFlutter. That is, I see no indication of regular atrial activity at a rate consistent with AFlutter. Instead, the rhythm is irregularly irregular without P waves = AFib at a controlled ventricular response. In my opinion, one doesn’t need Sgarbossa criteria here to activate the cath lab. So, yes the…
2018-09-13 02:09:24

Vince DiGiulioIs epinephrine harmful in cardiogenic shock?Sorry about that; I copied the quote from the article and my browser automatically changed the "μ" to an "m". Thanks for noticing, and thanks for pointing it out in the most passive-aggressive manner possible.
2018-09-12 16:45:26

Ken Grauer, MDElectrocardiographically Silent High Lateral STEMI EquivalentHi Tom. This is a great case — so NICE that you posted it for others to learned from. But as I commented several times when you sent this case around to our group — the T waves in V2,V3 are disproportionately peaked and transition occurs early (between V1-to-V2) — so the chest leads are NOT…
2018-08-14 08:38:03

Eli58 Year Old Male, Workout WorryAnybody else see the possibility of a LBBB or A-Flutter? I'm not sure if this will make any difference with the treatments but im just trying to interpret it first because if there is a LBBB then it does not meat Sgarbossa criteria and if it is A-Flutter that could explain the hyper acute T's…
2018-07-20 21:29:21